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A Structural Model for the Mass Action Kinetic Analysis of P-gp Mediated Transport Through Confluent Cell Monolayers
Book chapter

A Structural Model for the Mass Action Kinetic Analysis of P-gp Mediated Transport Through Confluent Cell Monolayers

Joe Bentz and Harma Ellens
Enzyme Kinetics in Drug Metabolism
01 Jan 2014
PMID: 24523118

Abstract

Biochemical Research Methods Biochemistry & Molecular Biology Life Sciences & Biomedicine Pharmacology & Pharmacy Science & Technology Toxicology
The structural model for P-gp mediated transport across confluent cell monolayers uses the generally accepted mass action reactions for P-gp binding and efflux, together with the known structural parameters for P-gp (large substrate binding site accessible from the membrane) and the apical plasma membrane in which it resides (lipid bilayer partition coefficient of substrate and volume of apical plasma membrane allow estimation of substrate concentration at binding site). The model considers binding of substrate to P-gp from within the inner leaflet of the apical membrane, with an on rate constant, k(1) (M-s(-1-1)), and off rate constant kr (s(-1)), as well as an efflux rate constant from P-gp into the apical chamber, k(2) (s(-1)). The model also explicitly estimates the active P-gp protein level, known as P-gp efflux active surface density T(0). For each new drug, fitting these parameters requires use of multiple initial drug concentrations and multiple time points at each concentration, until steady state is reached between P-gp-mediated efflux into the apical chamber and passive permeability from apical chamber back into the cytosol. Although this model optimally requires a larger than usual dataset for analysis, it does provide important mechanistic information through estimates of these on, off and efflux rate constants, as well as efflux active P-gp surface density. This more detailed description of efflux from polarized confluent cell monolayers has (1) provided insight into the unexpected relationship between P-gp IC50 and K-i in this system, (2) highlighted the kinetic need for GF120918 inhibitable apical and basolateral uptake transporters for digoxin, and (3) provided possible explanations for the extreme lab-to-lab variability in P-gp IC50 values observed for inhibition of digoxin transport. This model can also be used to distinguish between efflux active P-gp and total apical plasma membrane P-gp, which may be important when P-gp is expressed in a microvillous membrane.

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Collaboration types
Industry collaboration
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Web of Science research areas
Biochemical Research Methods
Biochemistry & Molecular Biology
Pharmacology & Pharmacy
Toxicology
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